Abstract 13024: Excessive Slow Flow and Thick Boundary Layers Cause Non ST Segment Elevation in Patients with Patent Coronary Arteries

Introduction: Many patients arrived to emergency room with atypical chest pain, borderline ST segment elevation, troponin level significantly elevated however the coronary angiogram was normal. Why? Hypothesis: Based on damages by flow disturbances in pipes, our research is built on the hypothesis that flow abnormalities disrupt delivery of oxygenated blood to the myocardium. Our strategy is to use today’s practice of fluid mechanics to unlock the mechanism of non-ST Segment elevation myocardial infarction (non-NSTEMI) and patent coronary arteries. What coronary flow abnormalities were the culprit? Methods: Patients with non-STEMI were enrolled if the coronary arteries were patent. In our new dynamic angiographic protocol, contrast was injected until the index coronary artery was completely opacified. Once the manual injection stopped, the blood moved in, displacing the contrast. The movements and directions of the blood flow in “white” color on top of a “black contrast” background could be clearly analyzed. The main focuses were the types of flows and their duration, direction and length. Results: 12 patients with non-STEMI and patent coronary arteries were enrolled. 100% patients had severe slow flow with prolonged arterial phase (>1.8secs) compared with historical control (0.72 secs) (p<0.05). 83% patients had retention flow with thick stagnant boundary layers at the proximal and mid segment of right coronary artery. The retrograde flow was short (0.18secs). Two patients showed excessive contraction of left ventricle. 4 patients revealed history of intense emotional stress however no sign of adrenergic excess (elevated blood pressure, heart rate or extreme peripheral vasoconstriction). All patients recovered and remained asymptomatic after one year follow-up. Conclusions: In non-STEMI and patent coronary arteries, severe slow flow and prolonged retention of thick boundary layers were the culprits. Besides the ischemia caused by delayed delivery of new blood to myocardium, the prolonged retention of thick boundary layers could prevent the intima from absorbing new oxygenated blood and provoked local ischemia. These new discoveries open new management and preventive options for patients with non-STEMI and patent coronary arteries.